Systemic & cornea/lens fundamentals Flashcards
Scleroderma
Bottom line: dry eyes + conjunctival telangiectasias + tight eyelid skin (or blepharophimosis) + malignant HTN retinopathy = SCLERODERMA
malignant hypertensive retinopathy: retinal hemorrhages, hard exudates, cotton wool spots, retinal and optic disc edema, and tortuous vessels.
rheumatic disease that occurs in localized/systemic forms
typically in women in their 30’s-50’s
Si/Sx: skin thickening and tightening and also by vascular insufficency and vasospasm (Raynaud’s phenomenon). Other systemic manifestions: GERD, pulmonary fibrosis, cardiac fibrosis, myositis, and renal disease (frequent cause of death and is commonly assoc/w/malignant HTN & kidney failure)
Mnemonic: Dr. Raynaud, a tight-fisted (tight eyelid skin) malignant (HTN) female attending (demographic) finding out she has scleroderma is mad (dry red eyes - conj telangiectasis). She is scarred down (cardiac/pulm fibrosis) and is going to die of kidney dz.
Which of the following findings is considered the hallmark of corneal limbal stem cell deficiency?
corneal limbal stem cells are located in the BASAL layer (“at the base”) of the limbus in a region called the “palisades of Vogt,” which are a series of fibrovascular ridges perpendicular to the corneal margin. These ridges are located approximately 1-2 mm posterior to the limbus where the conjunctiva and Tenons capsule fuse. These limbal stem cells divide asymmetrically to produce one daughter cell and one stem cell. Thus, the stem cell population remains static in healthy corneas. The daughter cells differentiate and migrate to replenish the corneal surface. The corneal epithelium is completely regenerated in approximately 7 days.
The hallmark of limbal stem cell deficiency (LSCD) is the PRESENCE OF GOBLET CELLS IN K EPITHELIUM (please commit this high yield fact to memory!). To demonstrate the presence of these cells, the clinician can either perform an excisional biopsy of the corneal surface or impression cytology and use a PAS or ALCIAN BLUE stain for goblet cells. Impression cytology is typically preferred since it is easier to perform and less invasive. Impression cytology basically involves pressing a piece of nitrocellulose filter paper against the corneal surface and staining whatever cells stick to the paper with the aforementioned dyes. The presence of conjunctival epithelial cells (or their markers; e.g. cytokeratin 19) on the corneal surface from impression cytology is another sign of LSCD.
Clinical signs of LSCD are:
“effacement” or loss of the palisades of Vogt,
late staining of the corneal epithelium with fluorescein,
peripheral pannus or corneal neovascularization
meds & corneal stromal deposits
Gold, phenothiazines, and retinoids are known to cause corneal stromal deposits.
Mnemonic: Rich person (gold) with bad skin (retinoids) who is crazy (phenothiazines), saying that he can’t see (K stromal deposits), when he actually can.
SLK
SLK: characterized by inflammation of the superior tarsal and bulbar conjunctiva (PAPILLARY reaction, not follicular), a fine punctate staining of the superior cornea/limbus, and filaments of the superior cornea. The superior bulbar conjunctiva is typically redundant, and one can slide this portion of the conjunctiva over the superior corneal surface with a cotton-tipped applicator.
Si/Sx: foreign body sensation, pain, and occasionally photophobia especially if filaments are present. The cause of SLK is not known, but it is associated with thyroid disease (typically hyperthyroidism), keratoconjunctivitis sicca, and hyperparathyroidism.
“mechanical” theory: thought that the rubbing of the superior palpebral conjunctiva against the superior bulbar conjunctiva (i.e. too much friction) causes the signs of SLK.
Rx: aggressive dry eye treatment, 0.5-1% silver nitrate SOLUTION (NEVER silver nitrate sticks which can cause burns) to the superior palpebral conjunctiva, resection of the redundant superior conjunctiva, pressure-patching, therapeutic contact lenses, and thermal cauterization.
Mooren’s ulcer systemic assoc
Mooren’s ulcer = Hepatitis C
Fabry’s disease
Fabry’s disease (X-linked alphagalactosidase deficiency). Sphingolipoides.
Fabry’s disease is characterized by renal failure, peripheral neuropathy, and hyperkeratotic skin lesions, and vortex keratopathy (which you can also see in amiodarone, indomethacin, chloroquine, and chlorpromazine).
Mnemonic: A Faberge egg (Fabry’s) with sparkles (vortex keratopathy). Alas, this is a bad gift (as is Tay-sachs - both spingolipioides), as it comes with skin/nerve problems and kidney disease. It too, like ichthyosis is X-rated (X-linked) and a fabulous hunter (fabry/hunter).
Superior limbic keratoconjunctivitis systemic assoc
Superior limbic keratoconjunctivitis = autoimmune thyroid disease
OCP
stereotypical: dz of older women (> 60 yo). Likely starts earlier in life and is not Dx due to early subtle findings. Stage 1: subepithelial fibrosis Stage 2: fornix foreshortening Stage 3: symblepharon formation Stage 4: corneal surface keratinization Stage 5: ankyloblepharon
Dx: conj bx with immunohistochemistry
supportive Dx: circulating autoantibodies (anti-beta4) to target antigen (beta 4 peptide of alpha-6-beta-4 integrin)
Cogan’s systemic assoc
Cogan’s syndrome (autoimmune interstitial keratitis and hearing loss) = polyarteritis nodosa
Mnemonic: Cogan the cyclops was blinded (interstitial keratitis). He couldn’t hear & had vertigo, he punched noodles (polyarteritis nodosa)
generally occurs in young adults who have had an upper respiratory tract infection in the previous 1-2 weeks.
Rx: Topical steroids for keratitis and oral steroids for the auditory system.
Important to rule out syphilis as a cause of the eye findings.
HSV vs. HZV
Zoster = nummular (“coin shaped” stromal infiltrates), raised mucous epithelial plaques weeks s/p skin rash, SECTORAL iris atrophy. Herpes also clasically gives the MOST NEUROTROPHIC keratopathy.
Mnemonic: older patients are more likely to be rich (coin shaped/nummular) and more likely to work for a SECTOR. Old = bad, so most neurotrophic keratopathy.
Simplex = no nummular infiltrates or plaques, PATCHY iris atrophy
Schnyder crystalline corneal dystrophy systemic assoc
Mnemonic: gene Ubi(AD)1. AD inheritance
Schnyder crystalline corneal dystrophy = hyperlipidemia / hypercholesterolemia
Central corneal opacification w/subepithelial crystals, dense arcus lipoides. RARE, progressive, affects STROMA at all levels starting in CENTER. Mid-periphery is LAST to become involved. decreased K sensation.
AD 2/2 mutation in UBIAD1 (Ubia prenyltransferase domain containing protein 1)
path: stains with oil red O stain
Dx: in 20s/30s. Better VA in scotopic conditions (dilated pupil)
Mnemonic: Eric Schynder (who is in his 20s/30s) riding in a red sports car (oil-red O) around a circle, which catches your peripheral vision (SPARES periphery, just like K blood staining clears periphery first). He is a rare progressive centrist with bad cholesterol (or lipid in balding hair). He likes Uber best [UBi(AD)1].
3 main sphingolipidoses
Fabry dz, multiple sulfatase deficiency, generalized gangliosidosis
All have corneal verticillata
Tay sachs is also a sphingolipidoses but typicaly has cherry red spot
tetracyclines SE
cause birth defects, permanent staining of teeth in children (< 10 years old contraindicated), and GI upset/diarrhea.
Epinephrine SE
SE: headache, palpitations, arrhythmias. Black deposits (oxidation rxns)
CME in aphakic pts
Mnemonic: aphakic patients get so excited (epi) that they can’t C (see/CME)
macular corneal dystrophy (MCD) mutation
defect in carbohydrate sulfotransferase 6 (CHST6)
K grafts
tissue storage < 4 days
death-to-preservation time: 12-18 hrs
endothelial count > 2K
Mnemonic: 4x3 = 12
Mutations in locusl 5q31 (TGFB1) cause:
granular (groenouw type I), Reis-Bucklers, lattice type I, Avellino
gelatinous droplike dystrophy mutation
defect in tumor associated calcium signal transducer 2 (TACSTD2)
AR
diffuse subepithelial and stromal amyloid deposits
VERY COMMON - recurrent errosions, and recurrence of the dz s/p transplant (nearly 100%)
How long to wait for transplantation of stem cells
1 year after chemical injury.
MC findng in sarcoidosis
calcific band keratopathy.
Other findings: nummular keratitis, thickening of DM, deep stromal vascularization 2/2 chronic uveitis
MC finding in sarcoidosis pts with ocular inv: periphlebitis; granulomatous uveitis with mutton fat KP (2/3 individuals with ocular involvement)
chronic angular blepharoconjunctivitis
crusting/ulceration of skin at lateral canthal angle.
Moraxella lacunata
papillary/follicular rxn of the tarsal conj
% of pts develop 2ndary glaucoma with ocular melanocytes
10%
HEDS study - stress
no STATISTICALLY significant assoc/w/HSV outbreaks and environmental stress
Average tear volume of an adult
7-10 uL
drop from standard medication - dispenses 50 uL per drop
Scleromalacia perforans
aka necrotizing scleritis WITHOUT INFLAMMATION (rare to have eye pain). ABSENT blood vessels overlying sclera with thinning.
assoc/w/RA - rheumatoid factor = autoantibody directed against IgG
HEDS- topical antiviral in stromal keratitis arm
Topical trifluridine eyedrops used to prevent an outbreak of herpetic epithelial keratitis.
Rx for stromal keratitis (autoimmune): PF q2h and topical trifluridine 4x/day.
No benefit in adding PO acyclovir to topical PF and trifluridine
Corneal blood staining clearance
clears centripetally = clears peripherally first, then moves to the center of the cornea. Esp concerning for amblyopa in kids
Mnemonic: Red bloody car (RBC) driving around a circle is likely to catch your PERIPHERAL vision (clears peripherally first)
conditions associated with limbal stem cell deficiency
Congenital aniridia
Ectodermal dysplasia, sclerocornea, KID syndrome*, congenital erythrokeratodermia**.
chem injury, S-J, trachoma, surgery.
Dx: goblet cells in epithelium (impression cytology)
stem cells live in the BASAL layer of the limbal epithelium. Need 25-33% intact to prevent conjunctival epithelium from growing onto the cornea.
Mnemonic: don’t KID around (KID syndrome) with a white cornea (scleroK)
- KID syndrome (keratitis-ichthyosis-deaf)
- *erythrokeratodermia: widespread hyperker @ birth
Riley-Day syndrome
aka Familial dysautonomia*. AR. Ashkenazi FH, skin blotching, neurotropic keratopathy with DECREASED tearing when crying.
On DDx for enlarged corneal nerves
Mnemonic: Ms. Riley Day, the Jewish girl who believes in her family, who gets on your nerves (K nerves) and no sensation (neurotrophia). Her skin gets BLOTCHY when she tries to cry crocodile tears (decreased tearing when crying). But don’t dismiss her b/c she has real problems (dysautonomia) even though she is quiet (AR).
*disturbs cells in the autonomic nervous system, which controls involuntary actions such as digestion, breathing, production of tears, and the regulation of blood pressure and body temperature
Mooren’s ulcer
“clasically” assoc/w/
- helminithic infection (parasitic warms = tapeworms, roundworms, flukes)
- hepatitis C
NO SCLERAL INVOLVEMENT (unlike PUK)
Mnemonic: Ms. Lauren (Mooren) with worms crawling all over her eyes. She also has hepatitis C. However, she is cosmetically conscious, so she wants white eyes (no scleral involvement)
ichthyosis and cornea changes
X-linked ichthyosis = form with corneal opacities
(less common with K changes but the MC type of ichthyosis = Ichthyosis vulagaris AD)
Mnemonic: X-rated ichthyotic patient to get K opacities
Indications for washout with hyphema
IOP > 60 mm Hg x 2 days
IOP > 35 mm Hg x 7 days
IOP > 25 mm Hg x 1 day in sickle-cell pt
Mnemonic: 60 x 2, 35 x 7, 25 x 1.
Think: 6023 and 5725-1
Lofgren syndrome
sarcoidosis
hilar adenonopathy, erythema nodosum, iridocyclitis
Mnemonic: Sarah Lofgren with hilar adenomathy, red bumps (erythema nodosum), uveitis and Sarcoid
Heerfordt syndrome
uveitis, parotitis, fever, CN7 palsy
Mnemonic: The uveitic feverish (fever) talking (CN7) parrot (parotitis) is “here for it” (heredordt).
assoc/w/MGD
Oral retinoid therapy rosacea DBUT (decreased break up time = faster tear breakup) posterior telangiectatic vessels keratin plugging hyperemia of the eyelid margin
contributes to majority of eye’s reractive power
air-tear interface = provides most of the optical power of the eye
Anterior K: 49 D
Posterior cornea: -6 D
Total K: 43 D
Refractive power of lens = 19
Aqueous component of tears
lacrimal glands, Krause and Wolfring glands
Mnemonic: Krouching wolf crying wolf
Nerve branches most affected by herpes zoster
Dermatomes of thorax (T3-L3)
Muir-Torre syndrome
hereditary disease in which patients present with MULTIPLE SEBACEOUS neoplasms (sebaceous adenomas or carcinomas) in conjunction with a VISCERAL MALIGNANCY usually of the GI or GU tract
Mnemonic: Dr. Muir has very fair skin and is thin: sebaceous adenoma/carcinoma, GI/GU tract
Erdheim Chester dz
subtype of xanthogranulomatous dz = infiltration of tissue (often in eyelid or orbit) when presenting with foamy histiocytes. often forming TOUTON GIANT cells. Rare dz but can be assoc/w/serious cardiac complications leading to death
Mnemonic: Chester the Giant, weights a TON (Touton). As a giant, he has heart problems.
Lesser-Trelat sign
Mnemonic: Think of Lestat, the vampire: He can’t go out in the sun (skin issues = many seborrheic keratoses) and issues feeding living off blood (GI adenocarcinoma). He is king (Keratin).
=sudden appearance of multiple seborrheic keratoses, usually indicates the presence of associated cancer (usually GI adenocarcinoma)
seborrheic keratosis = demonstrates a benign papillomatous proliferation of basal cells within the epidermis. Lesions OFTEN ALSO have a cystic collection of keratin
Cornea power and radius of curvature
contributes 75% of total dioptric power of a normal human eye
average radius of curvature of human cornea is 7.8 mm
Average dioptric power = 43
Below this endothelial count, patient is at greater risk of K edema after intraocular surgery
650 um
Coefficient of variation
(Standard deviation of the mean cell area)/(mean cell area)
Normal value < 0.3
Lymphoproliferative disorders
Variable ocular symptoms
Bone pain
Bruising
Slit-lamp exam: corneal deposits in epithelium or stroma
Rx: Supportive care
Refer to primary care physician
Medication-induced
Recent use of a topical fluoro-quinolone
Ocular irritation or photophobia
Slit-lamp exam: diffuse crystal deposit in cornea
Rx: discontinue gtts
Mnemonic: Fluoroquniolone = gyrating with crystals in the cornea
HSV vs HZV dendrites
HSV = TERMINAL BULBS and LOSS of epithelium HZV = tapered dendrites, raised lesion (pseudodendrites)
Mnemonic: Older patients are more refined (tapered ends), and believe in the importance of being raised well (raised lesion). More likely to be fake (psuedodendrites)
Disciform keratitis
2/2 endotheliitis. Oral acyclovir is thought to penetrate into the deeper corneal tissues through the aqueous and is used in addition to topical trifluridine (Viroptic) or topical gancyclovir (Zirgan) by some corneal specialists. Disciform keratitis secondary to HSV or VZV present the same. The overlying stroma and epithelium have edema in a round pattern.
purpose of the original HEDS study
(1) To evaluate the efficacy of topical corticosteroids in treating herpes simplex stromal keratitis in conjunction with topical trifluridine
(2) To evaluate the efficacy of oral acyclovir in treating herpes simplex stromal keratitis in patients receiving concomitant topical corticosteroids and trifluridine
(3) To evaluate the efficacy of oral acyclovir in treating herpes simplex iridocyclitis in conjunction with treatment with topical corticosteroids and trifluridine.
Mnemonic: stromal keratitis w/trifluridine x 2 - difference being +/-steroids and PO acyclovir. Then take PO acyclovir –> irdiocyclitis +steroids+trifluridine
Acyclovir: 400 2x/day (HSV; prophylactic),
800 mg 5x/day (HZV; acute), valtrex 1 gm tid.
acyclovir dose (prophylactic) against recurrence of herpes simplex is 400 mg po bid.
Typical treatment dosage of acyclovir for acute herpes zoster (including HZO) is 800 mg 5x/day for 7 to 10 days.
Alternative treatment regimens are frequently much more convenient (albeit more expensive) and include: (1) valacyclovir 1 gram tid for 7 days; (2) famciclovir 500 mg tid for 7 days; and (3) brivudin 125 mg qdaily for 7 days.
There is some suggestion that treatment of acute herpes zoster with valacyclovir is superior to acyclovir in preventing zoster-associated pain symptoms.
HSV stromal keratitis mediated by what cell from the immune system?
lymphocytes
High or low IOP in herpes?
Uveitis not due to Herpes (HSV and VZV) is typically accompanied by a decrease in pressure in contrast to the uveitis s een with Herpes, which typically has an increase in pressure. The elevation in IOP with Herpetic iridocyclitis is thought to be due to a trabeculitis which reduces aqueous outflow.
Uveitis secondary to other causes releases cytokines that increase uveoscleral outflow (which decreases pressure). In addition, uveitis from other causes typically results in ciliary body hyposecretion and thus decreased IOP.
Which nerve MC involved in HZV?
The ophthalmic division is most commonly affected in herpes zoster infection of the trigeminal nerve.
The ophthalmic division (i.e. CN V1) further divides into the nasociliary, frontal, and lacrimal branches. It is actually the FRONTAL BRANCH that is most commonly involved in herpes zoster infections. However, involvement of the nasociliary branch confers a higher risk of ocular involvement, 2/2 innervations of the nasociliary nerve with the eye (e.g. conjunctiva, sclera, cornea, iris, and choroid). The lacrimal branch is least commonly affected by HZV.
“Hutchinson’s sign” = when vesicles are present on the side of the tip of the nose. This sign indicates infection of the nasociliary nerve and thus a high likelihood of ocular involvement by HZV (i.e. herpes zoster ophthalmicus [HZO]).
To reiterate, the FRONTAL branch is most commonly involved by HZV infections, but involvement of the nasociliary branch is a stronger predictor of HZO.
Mnemonic: HZV is MC up FRONT (frontal branch of V1) about things, but if you have nasociliary branch you will want to cry (stronger predictor of HZO)
What path finding with chlaymida
Halberstaideter-Prowazek bodies are seen with chlamydial infections (think Trachoma). per wikipedia: Cytoplasmic inclusion bodies located near the nuclei of conjunctival epithelial cells in trachoma.
Mnemonic: Think of your polish-american (Prowazek), promiscuous college suitemate (chlamydia)
AIDS patient with PCP pneumonia and ocular irritation (conjunctivitis and epithelial keratopathy)
microsporidiosis: MC occurs in patients with AIDS or who are severely immunocompromised.
Si/Sx: conjunctivitis and epithelial keratopathy.
Dx: Scraping of the conjunctival epithelial cells with the Brown and Hopps stain will reveal small gram-positive spores.
Rx: Topical fumagillin
Mnemonic: tiny/micro AIDS patient with red irritated eyes (microsporidiosis; conjunctivitis and epithelial keratopathy) drinking beer (Brown Hopps stain) to feel positive (gram+)
Acanthamoeba keratitis
hallmark: pain that is out of proportion
typically begins as an epitheliopathy +/- pseudodendrites and perineural infiltrates (virtually pathognomonic)
ring infiltrate = late sign
trophozoites = highly sensitive but the cyst form is highly resistant to most forms of therapy
Currently, the diamidines and biguanides are the most effective antiamoebics available. The biguanides that are typically used are PHMB and chlorhexidine, of which PHMB is more commonly used. The diamidines include propamidine isethionate 0.1% and hexamidine 0.1%.
Which leads to a greater degree of decreased vision: surface or stroma irregularities?
Surface irregularities decrease vision to a greater degree than stromal changes.
Keratocytes: what type of cells? What do they do? Where are they most numerous? What happens with aging?
Keratocytes are modified fibroblasts = MC cell type in K stroma. They are found as flattened cells that are parallel to and between corneal lamellae. They are responsible for digesting and producing stromal molecules. They are more numerous in the anterior stoma and are least numerous posteriorly. Keratocyte population declines with age
Embryologically, these cells are derived from neural crest
cornea stroma
cornea stroma consists of an extracellular matrix of collagen fibrils and proteoglycans
types of collagen fibrils are type I, type V, and type VI
majority of corneal proteoglycans are derived from dermatan and keratan sulfate. There is a higher ratio of these proteoglycans in the posterior as compared to the anterior corneal stroma.
[156, dermatan/keratan] = posteriorly.
normal tear meniscus = convex or concave? What height? What is cut-off for abnml dry eye?
The normal tear meniscus (the fluid collection between the lower lid and the inferior cornea) is normally convex in shape and 1.0 mm in height. Heights of 0.3 mm or less are considered abnormal and a sign of dry eye.
Cornea vertex vs. apex
corneal vertex = point located at the INTERSECTION of the line of FIXATION and the corneal SURFACE
corneal apex = highest point in the cornea
Almost always, the corneal apex and the corneal vertex are NOT at the same point.
Relevant for refractive surgery since you should center your ablation around the corneal VERTEX.
Endothelial count and aging
4K cells/mm2 at birth.
“Young adults” ~3K cells/mm2. It decreases approximately linearly till the age of 60 when you have about 2,500 cells/mm2.
At that point, humans lose cells at a slower rate than when young. Thus, a 70- and 80-year-old would have more endothelial cells than you would think.
4K/3K/2.5K @60
Descemet’s
Unlike Bowman’s layer of the cornea, Descemet’s membrane is a true basement membrane. It serves as the basement membrane of the corneal endothelium and consists of type IV collagen fibrils. At birth, Descemet’s membrane is approximately 3-4 microns thick and increases in width to approximately 10-12 microns in adults. It is composed of two “zones”: (1) the anterior banded which develops in utero (darker line on path slide); and (2) a posterior nonbanded zone that is deposited by endothelial cells throughout life.
Remember “ABCD” = Anterior, Banded, Congenital, Does not grow
Sclera is made of what type of collagen.
The sclera is mostly made up of type I collagen and the proteoglycans, decorin, biglycan, and aggrecan. Type III collagen is associated with stromal wound healing. Type IV is associated with basement membranes (Descemet’s and lens capsule).
Mnemonic: Sclera is Type I collagen: the l in sclera is 1 .
Where does the cornea get glucose and oxygen?
The cornea is normally an avascular structure and it therefore depends on two main sources for its nutrition: (1) glucose from the underlying aqueous humor; and (2) oxygen diffusing through the tear film. The peripheral cornea does receive some oxygen from the limbal circulation.
UBM = how it works and what it does
High-frequency ultrasonography (also known as ultrasound biomicroscopy) uses a water-bath immersion tip. It is able to visualize 5 mm into opaque media. Structures posterior to the iris are able to be imaged with great accuracy (which includes the ciliary sulcus). This is the most accurate device for measuring sulcus-to-sulcus distances used to calculate lengths for phakic iols.
Scheimpflug cameras = how it works and what it does
Scheimpflug cameras (e.g. Pentacam) are mounted on a rotating arm (just like a slit lamp arm) and take 50 images of the cornea while rapidly rotating around (in about 2 seconds). The images are used as data points to generate anterior and posterior curvature maps, pachymetry maps, and anterior chamber depth.
For posterior curvature maps, they are more accurate than scanning-slit topographers because they take actual images of the posterior cornea. Scanning-slit topographers (e.g. Orbscan) have mathematically derived posterior curvature maps.
keratometer = how it works and what it does
MEASURES the anterior corneal curvature and ASSUMES the posterior corneal curvature to be a fixed constant.
The manual keratometer estimates corneal power by reading 4 points of the central 2.8-4.0 mm zone.
The instrument contains DOUBLING PRISMS to stabilize the image and therefore to allow more accurate focusing. The anterior corneal curvature is then obtained from the convex mirror formula and corneal power is calculated empirically using Snell’s law of refraction.
The keratometer uses an assumed index of refraction (1.3375 instead of the actual 1.376 of the anterior cornea) to account for the small contribution from the posterior corneal surface. The keratometer also assumes a standard corneal thickness and also ensures that 45 diopters of refracting power equals 7.5 mm radius of curvature (i.e. K (diopters) = 337.5/r).
Terrien marginal degeneration
Thin/Thirties/Top. with intact epi and lipid.
Traverse (leading edge of lipid), pannus over leading edge
Turns (is asymmetric)
Treatment is transplantation
u/L or asymmetric bilateral
cornea starts to thin superiorly and the thinning spreads circumferentially
intact epithelium and a fine pannus traverses the area of corneal thinning. At the end of the pannus is a line of lipid deposition.
Corneal steepening occurs 90 degrees away.
Perforation of the thinned cornea is rare. Crescent shaped lamellar transplantation can be used if perforation does occur
The epithelium remaining intact distinguishes Terrien from other diseases such as Mooren ulcer and PUK (peripheral ulcerative keratitis which have loss of epithelium. Also, Terrien does not have pain because there is no loss of epithelium.
iron lines in cornea
“Ferry’s line” at the leading edge of a filtering bleb, “Fleisher ring or line” surrounding the base of a cone in keratoconus, and “Stocker’s line” at the leading edge of a pterygium.
Biomechanics/Q value:
Biomechanics/Q value: approximately 200 parallel lamallae more packed in the anterior 2/3 asphericity of the K = Q value Q = 0 for spherical K Q> 0 for oblate K Q< 0 for prolate K
If you are pro, you can do more with less (into negative value = prolate)
Normal K = prolate, Q = -0.26 (think my birthday)
K becomes more oblate (with steeper peripheral K) after refractive surgery
Which corneal vital dye is toxic
Think rose Bengal: like a rose, with thorns (toxic)
fluorescein -used to detect disruption of intercellular junctions; e.g. which occurs in corneal epithelial defects.
Fluorescein is also used to measure “tear breakup time” (TBUT) and for applanation tonometry.
Rose Bengal and lissamine green stain devitalized cells or when a disruption occurs in the overlying mucin coat. They are most commonly used to assess dry eye states. Rose Bengal is much more irritating to the ocular surface as compared to either lissamine green or fluorescein.
The slit-lamp photo depicts the classic dendrites of HSV epithelial keratitis which have been stained with rose bengal. Unlike fluorescein dye which stains epithelial basement membrane (e.g. in epithelial defects), rose bengal preferentially stains dead/devitalized corneal epithelial and conjunctival cells.
Rose bengal binds equally well to virally-infected and non-infected devitalized cells and has the ability to inhibit HSV replication.
Iodine %?
Generally, iodine comes as a 10% solution. This is toxic to the corneal epithelium and must be diluted 50% to make a 5% solution. The fornix should be cleaned with this 5% solution. It has been shown to reduce bacterial load in the eye after cataract surgery.
peripheral corneal guttae
Hassall-Henle bodies
Cowdry bodies
Cowdry bodies are eosinophilic nuclear inclusions composed of nucleic acid and protein seen in cells infected with herpes simplex virus, varicella-zoster virus, and cytomegalovirus.
Viruses are such COWs
Schwalbe’s line
Schwalbe’s line is the posterior most extension of Descemet’s membrane.
Bowman’s Layer Type of collagen
Bowman’s Layer is primarily Type 1 and 5 collagen.
sclera Type of collagen
The sclera is mostly made up of type I collagen and the proteoglycans, decorin, biglycan, and aggrecan.
three predominant GAGs
3 predominant GAGs that are found in the K stroma are: keratan sulfate, chondroitin sulfate, and dermatan sulfate.
GAGs = long, unbranched polysaccharides that consist of a repeating disaccharide unit. They are negatively-charged and are usually associated with a small amount of protein to form proteoglycans. GAGs bind large amounts of water and therefore form gel-like structures (e.g. vitreous). They are classified into distinct groups based on the core disaccharide unit:
Chondroitin sulfates:
Chondroitin sulfates: most abundant GAG in body; found in cartilage, bones, tendons, and ligaments
Keratan sulfates:
Keratan sulfates: found in cornea and other connective tissue
Dermatan sulfates:
found in skin, blood vessels, tendons, lungs
Heparins/heparan sulfates
involved in coagulation, angiogenesis, developmental processes
Hyaluronates
skin, cartilage, vitreous
hyperlipoproteinemia
Frederickson type I disease is a type of hyperlipoproteinemia. LCAT deficiency, Fish eye disease, and Tangier disease are examples of hypolipoproteinemias. All of these diseases are associated with accumulation of lipid. The hypolipoproteinemias are so named because they have a deficiency of the so called good cholesterol (HDL) that is responsible for removing the bad cholesterol.
Schirmer:
Schirmer:
Think basic: always use + anesthetic
Think Schirmer 1: don’t know what is going on so he doesn’t use anesthetic
Think Schirmer 2: 2nd try, + anesthetic! messing around with the nose
All of these tests measure absorption of tears by a paper strip at 5 minutes.
basic secretion test
consists of placing a drop of topical anesthetic on the eye of interest. This is followed by blotting off any excess fluid in the tear meniscus. A standard-size filter-paper is then placed at the junction of the middle and lateral thirds of the lower eyelids. The amount of wetting of this filter-paper at 5 minutes is recorded. “Abnormal” values are wetting less than 5 mm while “equivocal” values measure 5-10 mm.
<5
Schirmer I
The Schirmer I test is performed exactly like the basal secretion test except that it does not use a topical anesthetic. Therefore, theoretically, the Schirmer I test measures BOTH BASAL AND REFLEX tear production. Wetting of the filter paper of less than 10 mm at 5 minutes is considered abnormal.
<10
Schirmer II
The Schirmer II is performed like the Schirmer I test (i.e. no topical anesthesia), except that the nasal mucosa is simultaneously stimulated with a COTTON TIP APPLICATOR. Wetting values less than 15 mm at 5 minutes is considered abnormal for the Schirmer II test. There are no tests of tear production called the “Schirmer IV” or “lacrimal function” tests.
<15
Thygeson superficial punctate keratitis.
classic presentation: photophobia, FBS in the presence of a cluster of corneal epithelial lesions which stain “negatively” with fluorescein. In addition, both eyes are affected and the lesions are concentrated centrally on both corneas.
etiology=unknown
best initial Rx:ATs especially in mild-to-moderate cases. The corneal lesions are very sensitive to steroid treatment but have a high rate of recurrence once the drops are stopped. Conservative treatment is the best first-line approach. Cyclosporine eyedrops (i.e. Restasis®) are also effective and are sometimes preferred over steroids due to their higher safety profile.
enlarged K nerves
men(2)larged K nerves MEN IIb NF2 Leprosy Acanthomoeba Refsum Glaucoma (congenital) Edema (of the cornea) Dysautonomia (Riley-day)
Only cells present in normal conjunctiva
plasma cells
Can find VEGF where?
In the tear film of inflammed eyes
Cornea immune privilege due to..
Fas ligand (CD95 lignad) by cornea cells. thought to be critical in apoptosis (programmed cell death of activated lymphocytes)
Prominent nerve DDx?
- MENIIB
- Keratoconus
- Ichthyosis
- Fuchs corneal dystrophy
- Corneal edema
- Congenital glaucoma
Verticillatta DDx?
– Amiodarone – Fabry disease – Indomethacin – Phenothiazine – Chloroquine – Chlorpromazine
BCL’s Dk and fit?
Want high Dk (high oxygen transmission)
Want tight fit so lens doesn’t move with blinking
